Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Necrotizing enterocolitis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources
PubMedDate not supplied

[Linezolid in two premature babies with necrotizing enterocolitis and infection with vancomycin-resistant enterococcus].

The use of the antibiotic Linezolid in two premature babies with necrotizing enterocolitis and infection with vancomycin-resistant enterococcus is described. Therapy with Linezolid in cause of necrotizing enterocolitis is an exception. Actually there are no proven recommendations for the use in this age group. Despite the successfully results more investigations for the use of linezolid in newborns and prematures are necessary.

Acetamides↗
PubMed2003

Early feeding after necrotizing enterocolitis in preterm infants.

OBJECTIVE: To report our experience with an early initiation of enteral feedings after necrotizing enterocolitis (NEC). STUDY DESIGN: Over a 4-year period, all inborn infants with NEC Bell stage II or greater received enteral feedings, increased by 20 mL/kg/d, once no portal vein gas had been detected on ultrasound for 3 consecutive days (group 1). Infants were compared with a historic comparison group (group 2). RESULTS: Necrotizing enterocolitis rates were 5% (26/523) in the early feeding group and 4% (18/436) in the comparison group. One early feeding infant and two comparison group infants died of NEC, whereas two and one, respectively, had recurrent NEC. Enteral feedings were restarted at a median of 4 days (range, 3-14) versus 10 days (range, 8-22) after onset of NEC. Early feeding was associated with shorter time to reach full enteral feedings (10 days [range, 7-31] vs 19 days [range, 9-76], P<.001), a reduced duration of central venous access (13.5 days [range, 8-24] vs 26.0 days [range, 8-39], P<.01), less catheter-related septicemia (18% vs 29%, P<.01), and a shorter duration of hospital stay (63 days [range, 28-133] vs 69 days [range, 36-150], P<.05). CONCLUSION: Early enteral feeding after NEC was associated with significant benefits and no apparent adverse effects. This study was underpowered, however, to exclude a higher NEC recurrence risk potentially associated with this change in practice.

Enteral Nutrition↗
PubMed1999

Characteristics of protein and energy metabolism in neonates with necrotizing enterocolitis--a pilot study.

BACKGROUND/PURPOSE: It is assumed that neonates with necrotizing enterocolitis (NEC) are hypermetabolic. However, the dynamics of protein and energy metabolism in neonates with NEC have not been characterized. The purpose of this study was to test the hypothesis that protein turnover and energy expenditure are increased during the acute stage of NEC and later return to normal values. METHODS: A pilot study was performed on six neonates with proven NEC (Bell's stage II or III). Patients were studied in two phases: (1) in the acute stage of their disease and (2) when their clinical condition had stabilized. Whole-body protein turnover was calculated using an intravenous infusion of [1-13C] leucine and by measuring the isotopic enrichment of plasma [13C]alpha-ketoisocaproic acid and 13CO2. Respiratory gas exchange was measured simultaneously by computerized indirect calorimetry. RESULTS: Median gestational age was 36 weeks (range, 28 to 40) with a median postnatal age of 21 days (range, 6 to 47). All patients recovered from the acute episode, although three patients died after recovering from the acute disease from other conditions. The patients studied showed marked variability in protein metabolism kinetics. However, there was no difference in whole-body protein flux between the acute phase (7.6 g/kg/d; range, 5.6 to 18.2) and the recovery phase (7.0 g/kg/d; range, 6.9 to 12.2; P = .89). Furthermore, there was no difference in any of the component parts of wholebody protein turnover. Resting energy expenditure did not change between the acute phase (42.8 kcal/kg/d; range, 34.4 to 52.5) and the recovery phase (51.0 kcal/kg/d; range, 34.9 to 55.3; P = .18). CONCLUSIONS: This pilot study shows that the rates of protein and energy metabolism in neonates with NEC are comparable with reported values in stable neonates. There was no difference in protein or energy dynamics between study phases. The authors speculate that neonates with NEC may divert the products of protein synthesis from growth to tissue repair.

Calorimetry, Indirect↗
PubMed2002

T cryptantigen activation is associated with advanced necrotizing enterocolitis.

BACKGROUND/PURPOSE: Thomsen-Friedenreich cryptantigen activation (TCA) exposes neonates with necrotizing enterocolitis NEC to the risk of hemolysis after transfusion of blood products. The authors aimed to determine the prevalence of TCA in neonates with NEC and to correlate TCA with severity of disease and outcome. METHODS: One hundred four neonates with NEC were tested for TCA on admission. Patients with TCA requiring transfusion were given packed red cells, low-titer anti-T fresh frozen plasma, and washed platelets to avoid hemolysis. RESULTS: Twenty-three infants had TCA, and 96% of these had stage III disease. The incidence of TCA was significantly higher in infants with stage III disease compared with those with stage II (30% v 4%; P <.01). A total of 91% of infants with TCA required laparotomy compared with 81% of those with no activation. At laparotomy, widespread disease was more common in the TCA group (71% v 55%). TCA did not significantly increase mortality rate (TCA, 39% v no TCA, 28%); this may reflect the transfusion policy of our unit. CONCLUSIONS: Twenty-two percent of neonates with NEC referred to our unit had TCA. There is an association between TCA and advanced NEC. Screening of neonates with advanced NEC for TCA is advised to identify those at risk of hematologic complications.

Antigens, Tumor-Associated, Carbohydrate↗
PubMed2002

A study of gut immunity to enteral endotoxin in rats of different ages: a possible cause for necrotizing enterocolitis.

PURPOSE: Immature gut immunity can be a predisposing factor for necrotizing enterocolitis (NEC). The gut active immunity and innate defense to the Escherichia coli endotoxin lipopolysaccharide (LPS) in immature and mature rats were studied. METHODS: LPS, started at a dose of 10 mg/kg, was instilled into the stomachs of fetal, newborn, 1-month and 3-month-old rats. Boost doses and normal saline control instillations were given on day 14. Rats that died after instillation had detailed postmortem examinations. For survivors, a group of 6 immunized and 6 controls were killed on day 7 for the collection of serum, spleens, mesenteric lymph nodes, and small intestines. Lymphocytes (10(6)) prepared from each tissue sample of individual group were cultured for 5 days. Serum and supernatant were analyzed for IgA and anti-E coli IgA levels. RESULTS: All control rats survived. The doses of LPS given were 10, 5, 2.5, and 1.25 mg/kg. All fetal rats died after LPS instillation. Half-lethal dose for newborns was 2.5 mg/kg. One-month and 3-month-old rats survived all doses of LPS. The cause of death was endotoxemia. The serum IgA and total supernatant anti- E coli IgA levels of rats of all ages studied showed no significant difference. CONCLUSION: The poor innate gut defense, not so much the active immunity, may provide an explanation for the susceptibility of the premature babies and newborn infants to the development of NEC.

Animals↗
PubMed2003

Erythropoietin protects against necrotizing enterocolitis of newborn rats by the inhibiting nitric oxide formation.

BACKGROUND: Necrotizing enterocolitis (NEC) is an important neonatal disease with a high mortality rate; erythropoietin (Epo) is a hematopoietic growth factor. Functional Epo receptors are in the fetal and postnatal small bowel and their ligands are available for binding. Excessive nitric oxide (NO) production by an isoform of NO synthase inducible by inflammatory stimuli leads to changes in vascular permeability and tissue injury. The aim of this study was to investigate NO formation in an experimental model of NEC and the possible role of NO in the protection Epo provides against NEC. METHODS: Twenty-four Wistar albino rat pups were divided into three groups: group 1 = control; group 2 = hypoxia-reoxygenation and saline; group 3 = hypoxia-reoxygenation and recombinant human EPO (rhEpo) pretreatment. rhEpo was given 750 U/kg/week by intraperitoneal injection 3 times a week for 2 weeks. On the 15th day, hypoxia was induced by placing the pups in a 100% CO(2) chamber for 5 min. After the hypoxia period the pups were reoxygenated for 10 min with 100% O(2) and returned to their mothers. All pups were killed 4 h after the hypoxia-reoxygenation period was over. The abdomen was opened and representative samples of injured areas were taken for histopathologic examination. Then nitrite levels were determined in the intestine by Griess Reagent. RESULTS: On histopathological examination, injury scores in group-2 animals were found to be significantly higher than in group-3 animals (p = 0.001). Significantly increased intestinal nitrite levels were found in group-2 rats compared to the rats of groups 1 and 3 (p = 0.001 and p = 0.001, respectively). There was a positive correlation between the histological findings and the intestinal nitrite levels in group-2 and -3 animals (r = 0.94, p = 0.001; r = 0.99, p = 0.001, respectively). CONCLUSION: The present study demonstrates that the Epo-pretreated group had decreased levels of NO and limited mucosal necrosis in intestinal tissue samples. We believe that these results deserve further experimental studies in order to elucidate the possible effector mechanisms involved in the inhibitory relationship between Epo, NO and NEC.

Animals↗
PubMed2003

Maternal milk reduces severity of necrotizing enterocolitis and increases intestinal IL-10 in a neonatal rat model.

Necrotizing enterocolitis (NEC) is a devastating intestinal disease of premature infants. Maternal milk has been suggested to be partially protective against NEC; however, the mechanisms of this protection are not defined. The aim of this study was to examine the effect(s) of artificial feeding of rat milk (RM)-versus cow milk-based rat milk substitute (RMS) on the development of NEC in a neonatal rat model and elucidate the role of inflammatory cytokines in NEC pathogenesis. Newborn rats were artificially fed with either collected RM or RMS. Experimental NEC was induced by exposure to asphyxia and cold stress and evaluated by histologic scoring of damage in ileum. Intestinal cytokine mRNA expression was determined by real-time PCR. Cytokine histologic localization was performed by confocal microscopy. Similar to human NEC, artificial feeding of RM reduces the incidence and severity of NEC injury in neonatal rats. Freezing and thawing of collected RM did not eliminate the protective effect of maternal milk. Ileal IL-10 expression was significantly increased in the RM group compared with RMS. Increased IL-10 peptide production was detected in the RM group with signal localized predominantly in the cytoplasm of villus epithelial cells. These results suggest that the protective effect of maternal milk is associated with increased production of anti-inflammatory IL-10 in the site of injury. Better understanding of the mechanisms underlying these protective effects could be beneficial either in the prevention of NEC or in the development of future therapeutic strategies to cure NEC.

Animals↗
PubMedDate not supplied

Evidence of TNF system activation and high expression of TNF alpha messenger transcripts in necrotizing enterocolitis of HIV-infected children.

TNF alpha contributes to the necrotizing enterocolitis (NEC) pathogenesis. To date, this clinical entity of neonates was never described in HIV-infected children. In 15 HIV-positive children with histological evidence of various intestinal lesions resembling NEC, we have studied serum TNF alpha and soluble TNF receptor concentrations by ELISAs, and archived paraffin embedded intestinal tissues by in situ hybridization with DIG-labeled RNA probes for TNF alpha messenger transcripts. We found increased levels of TNF alpha and soluble receptors, proving TNF alpha system activation. We detected TNF alpha messenger transcripts in all cases, regardless of the presence of microbial pathogens at intestinal level. Since HIV can infect many cells of the gastrointestinal tract, also triggering the secretion of TNF alpha, we concluded that factors contributing to NEC pathogenesis in HIV-infected children are complex. At least the nutritional and immunological status are involved, other viral co-infections, opportunistic microbes (such as mycobacteria), and pathogenic activities of HIV. All together enhance both circulating TNF alpha system and its cytotoxic effects at intestinal level.

Antigens, CD↗
PubMed2003

Microbiological factors associated with neonatal necrotizing enterocolitis: protective effect of early antibiotic treatment.

AIM: The incidence of necrotizing enterocolitis (NEC) strongly increased in an neonatal intensive care unit (NICU) in 1997 and 1998 compared with previous years, which coincided with increased incidence of nosocomial sepsis. Specific risk factors related to this NICU and a possible relationship between NEC and nosocomial sepsis were studied retrospectively, including all patients with NEC since 1990 and matched controls. METHODS: Clinical and bacteriological data from the period before the development of NEC and a similar period for the controls were collected retrospectively and corrected for birthweight and gestational age. Statistical analysis was performed by a stepwise regression model. RESULTS: Data of 104 neonates with NEC and matched controls were analysed. The median day of onset of NEC was 12 d (range 1-63 d). Significant risk factors for NEC were: insertion of a peripheral artery catheter [odds ratio (OR) 2.3, 95% confidence interval (95% CI) 1.3-3.9] and a central venous catheter (OR 5.6, 95% CI 3.1-10.1), colonization with Klebsiella sp. (OR 3.4, 95% CI 1.5-7.5) and Escherichia coli (OR 2.1, 95% CI 1.0-4.5), and the occurrence of sepsis, in particular due to coagulase-negative staphylococci (OR 2.6, 95% CI 1.4-5.1). The risk for NEC was decreased after the early use (< 48 h after birth) of amoxicillin-clavulanate and gentamicin (OR 0.3, 95% CI 0.2-0.6). CONCLUSION: Insertion of central venous and peripheral arterial catheters is positively associated with NEC, as is colonization with the Gram-negative bacilli Klebsiella and E. coli and the occurrence of sepsis, particularly due to coagulase-negative staphylococci. Early treatment with amoxicillin-clavulanate and gentamicin is negatively associated with NEC and may be protective against NEC.

Anti-Bacterial Agents↗
PubMed2006

Platelet transfusions in infants with necrotizing enterocolitis.

Severe thrombocytopenia (< 50 x 10(9)/L) frequently accompanies advanced necrotizing enterocolitis (NEC). In premature infants with severe thrombocytopenia, despite a paucity of evidence to support the practice, platelet transfusions are commonly used to maintain arbitrary levels of platelet counts in an effort to prevent hemorrhage. However, platelet transfusions contain a variety of bioactive factors, including platelet activating factor (PAF), which can augment systemic inflammatory processes. A growing body of evidence that incriminates PAF in the pathogenesis of NEC has emerged over the past few decades from both animal and human data. Both severe thrombocytopenia and multiple platelet transfusions have been associated with increased mortality, but it is admittedly difficult to differentiate between the effects of the underlying disease and the effects, if any, of the platelet transfusions. In this report, we review the roles of PAF and platelet transfusions in infants with severe NEC.

Enterocolitis, Necrotizing↗
PubMed1997

Nitroglycerin attenuates the bowel damage of necrotizing enterocolitis in a rabbit model.

Endogenous enteric nitric oxide has multiple functions. Enteric nitric oxide may be diminished in the premature infant and may therefore predispose the immature intestine to injury. The aim of this study was to determine if the infusion of a nitric oxide donor (nitroglycerin) would attenuate intestinal damage in a rabbit model of necrotizing enterocolitis. Transmural injection of rabbit intestinal loops with an acidified solution of casein and calcium gluconate simulates certain aspects of necrotizing enterocolitis. After injection of acidified casein solution into rabbit intestinal loops, twelve rabbits were randomly divided into two groups: six received maintenance fluids only and six received maintenance fluids and a nitroglycerin infusion adjusted to maintain mean arterial pressure 10 mm Hg below baseline (range, 2 to 12 micrograms/kg/min). After 3 hours, the rabbits were killed, and the intestinal tissue graded histologically. Intestinal damage in the nitroglycerin-treated rabbits was significantly less than that of untreated controls (mean histological grade of 0.39 v 1.48, P < .001). In this rabbit model of necrotizing enterocolitis, infusion of the nitric oxide donor nitroglycerin significantly attenuates intestinal damage. We speculate that enteric nitric oxide deficiency, as may exist in the preterm infant, predisposes the intestine to necrotizing enterocolitis.

Animals↗
PubMed1980

Mild form of neonatal necrotizing enterocolitis masked by anal fissures.

In three infants with clinically mild necrotizing enterocolitis, heme-positive stools were initially attributed to anal fissures, delaying diagnosis and treatment of the enterocolitis for 4-10 days. Radiographically, pneumatosis intestinalis involved the entire colon and rectum. A causal relation may exist between necrotizing enterocolitis and anal fissure.

Enterocolitis, Pseudomembranous↗
PubMed1988

Neonatal rotavirus-associated necrotizing enterocolitis: case control study and prospective surveillance during an outbreak.

After the death of a premature infant from rotavirus-associated necrotizing enterocolitis, we instituted prospective surveillance for this disease in our neonatal intensive care unit. During the 4-month study period an additional six cases of necrotizing enterocolitis and eight cases of hemorrhagic gastroenteritis occurred. Rotavirus infection was documented in 11 of these 15 symptomatic infants, in comparison with only eight rotavirus infections in 147 asymptomatic or minimally symptomatic babies (P less than 0.0001). Stools from 110 nursery personnel tested during the outbreak did not contain rotavirus. However, 12 of 59 staff members had serum IgM antibody against rotavirus, suggesting recent infection. In a case-control study we compared babies with severe gastrointestinal illness with a control group randomly selected from asymptomatic babies in the nursery during the time of the outbreak. Univariate analysis found six categorical variables and nine continuous variables that were significantly associated with disease. Multivariate logistic regression analysis, however, found only birth weight (P less than 0.0001), rotavirus infection (P less than 0.0001), and age at time of first nonwater feeding (P less than 0.02) to be associated with gastrointestinal illness. This study provides further evidence for the role of infection in some cases of neonatal necrotizing enterocolitis and hemorrhagic gastroenteritis.

Colorado↗
PubMed1990

Prevention of neonatal necrotizing enterocolitis.

Small premature infants are often hypochlorhydric, and frequently their stomachs are colonized by enteric, gram-negative bacteria. We tested a hypothesis that gastric pH affected the colonization of the stomach with enteric bacteria and that this colonization was causally related to the risk or severity of necrotizing enterocolitis. A prospective, double-blind study was conducted that compared a group of infants supplemented with 0.01-0.02 ml of 1 N HCl/ml of milk to a group with a similar supplement of water. Gastric pH, gastric enteric bacteria counts, and the incidence and severity of necrotizing enterocolitis were monitored. The median gastric pH of the HCl-supplemented group was lower (3.0) than controls (4.0) throughout the study (p less than 0.001). The gastric enteric bacterial colonization rate and the quantitative bacterial counts were strongly correlated with gastric pH over 4 (p less than 0.001). Somatic growth rates in infants in the HCl-supplemented group were equal to, or exceeded, those in the control group. There was 1 case of necrotizing enterocolitis among the 34 infants in the HCl-supplemented group and 8 cases among the 34 in the control group (p = 0.02). It appears that acidifying the feedings of small premature infants to a pH low enough to inhibit bacterial proliferation in the stomach significantly lowers the risk of necrotizing enterocolitis.

Animals↗